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1 he beta-catenin pathway, is downregulated by clofibrate.
2 f the older fibrates such as gemfibrozil and clofibrate.
3 le to inhibition by the antilipid medication clofibrate.
4 ding mice for 2 weeks with a diet containing clofibrate (0.5%, w/w), a PPAR alpha ligand and peroxiso
5 brassinosteroid, salicylic acid), chemicals (clofibrate, 1-aminocyclopropane-1 carboxylic acid), or e
6 nts with hypertriglyceridemia were placed on clofibrate, 2 g/day for 12 months.
7                                              Clofibrate, 3-methylcholanthrene, or beta-naphthoflavone
8                               Moreover, both clofibrate, a peroxisome proliferator-activated receptor
9              Here, we examine the effects of clofibrate, a representative of the fibrate class, on re
10  immunoprecipitation analysis confirmed that clofibrate abrogates the binding of nuclear factor-kappa
11 he PPARalpha, oleic acid, linoleic acid, and clofibrate, accelerated epidermal development, resulting
12 ed from FABP binding changes suggesting that clofibrate also enhances fatty acid diffusion within int
13                   Finally, topically applied clofibrate also increased apoptosis.
14 xyl phthalate, ciprofibrate ethyl ester, and clofibrate also resulted in tyrosine phosphorylation of
15                                              Clofibrate and 9-cis-retinoic acid, the partner ligands
16  in response to the peroxisome proliferators clofibrate and di(2-ethylhexyl) phthalate.
17 cts were observed in explants incubated with clofibrate and farnesol together in suboptimal concentra
18              Further, the PPARalpha ligands, clofibrate and GW4647, and various xenobiotic carboxylic
19 wo distinct ligands of PPAR-alpha (including clofibrate and WY 14643) also cause a substantial reduct
20    In this study we determined the effect of clofibrate and Wy-14,643, activators of PPARalpha, on hy
21            We found that PPAR alpha ligands (clofibrate and WY14643) enhanced IL-1 beta-induced COX-2
22 ent with two different PPARalpha activators, clofibrate and WY14643, accelerated the postnatal declin
23 liferators di(2-ethylhexyl)phthalate (DEHP), clofibrate, and 4-chloro-6-(2,3 xylidino)-2-pyrimidinylt
24 The PPs Wy-14643, mono-ethylhexyl phthalate, clofibrate, and ciprofibrate ethyl-ester were found to b
25 c PPARalpha ligands Wy-14,643, ciprofibrate, clofibrate, and others induce the nuclear translocation
26                      Similar to gemfibrozil, clofibrate, another fibrate drug, also inhibited the exp
27 dy showed that PANC1 xenografts treated with clofibrate are more sensitive to radiation than untreate
28               In the central nervous system, clofibrate blocked nicotine's effects on neuronal firing
29 rator-activator receptor (PPAR) alpha ligand clofibrate but not the PPARgamma ligand troglitazone, su
30  by treating mice with the PPARalpha agonist clofibrate, but not from the analysis of PPARalpha knock
31 The PPs Wy-14643, mono-ethylhexyl phthalate, clofibrate, ciprofibrate ethyl ester, and eicosatetrayno
32 l hepatocyte cultures with either ethanol or clofibrate demonstrated a 2-fold increase in CYP2E1 leve
33 T) with peroxisome proliferators, WY 14,643, clofibrate, di(2-ethylhexyl) phtalhate, and acetylsalicy
34                                    Moreover, clofibrate did not significantly alter ear thickness fol
35                                              Clofibrate eliminated MCD-mediated hepatic steatosis but
36                                              Clofibrate feeding increased the amount of RRD protein i
37 d in male rats by a diet containing DEHP and clofibrate for 3-60 days.
38                           Male rats were fed clofibrate for 9 days to increase the hepatic concentrat
39 rate that PPARalpha-selective ligands (i.e., clofibrate, GW7647) significantly induce BCRP mRNA and p
40 bital (PB), beta-naphthoflavone (betaNF), or clofibrate in a mouse model increased ROS parameters in
41  efficacy of ursodeoxycholic acid (UDCA) and clofibrate in the treatment of NASH.
42                               Treatment with clofibrate increased FABP levels, the fraction of NBD-st
43 aim was to determine if induction of FABP by clofibrate increases the cytoplasmic transport of a fluo
44               Peroxisomal proliferators like clofibrate induce FABP and may stimulate fatty acid use
45              In contrast, neither DHEA-S nor clofibrate induced these hepatic proteins and mRNAs in P
46                                              Clofibrate-induced expression of kidney CYP4A mRNAs was
47 000 g fraction of liver, consistent with the clofibrate-induced increase in reductase activity.
48                                 Furthermore, clofibrate inhibition of humanized TAS1R3 in the genetic
49  Despite the known lipid-lowering effects of clofibrate, it did not appear to be of clinical benefit
50                                              Clofibrate-mediated induction of SCD1 mRNA was shown to
51 erexpressed in pancreatic cancer tissues and clofibrate-mediated PPARalpha activation sensitizes panc
52              Among the patients treated with clofibrate, no change from baseline was found in mean AL
53                       Nonspecific effects of clofibrate on cytoplasmic viscosity or pore size were no
54  the antagonist GW6471 abolish the effect of clofibrate on radiosensitization.
55 ce that had been fed diets supplemented with clofibrate or gemfibrozil.
56  peroxisome proliferator-activated receptor (clofibrate or linoleic acid), farnesoid X-activated rece
57 azid, pregnenolone 16alpha-carbonitrile, and clofibrate) or the general P450 inhibitor 1-aminobenztri
58 e specific activity and units indicates that clofibrate/PPAR alpha induced expression of retinal-redu
59                                              Clofibrate prevented the acquisition of nicotine-taking
60 itation analysis indicated that both DHA and clofibrate reduce HIF-2alpha binding to the HRE.
61 ved that PPARalpha activation by its agonist clofibrate sensitizes pancreatic cancer cells to radiati
62                               Treatment with clofibrate significantly accelerated normalization of ba
63 ns Clofibrate Study, the Newcastle upon Tyne Clofibrate Study, and the Pravastatin Limitation of Athe
64                      The Scottish Physicians Clofibrate Study, the Newcastle upon Tyne Clofibrate Stu
65 xyl phthalate, ciprofibrate ethyl ester, and clofibrate suggested that they may be activating growth-
66 accumulation by monolayer cells treated with clofibrate, suggesting increased BCRP efflux activity.
67 in intact animals, we administered DHEA-S or clofibrate to mice lacking a functional PPAR alpha gene.
68                                     Finally, clofibrate treatment also reduced ear thickness and weig
69                            Moreover, topical clofibrate treatment did not increase epidermal differen
70 e polymerase chain reaction, we observe that clofibrate treatment increases PPARalpha binding to the
71                                In the other, clofibrate treatment induced ER redistribution of matrix
72                      These data suggest that clofibrate treatment induces cytosolic FABP and stimulat
73 taining in the epidermis that was reduced by clofibrate treatment.
74                                              Clofibrate was found to induce liver SCD1 mRNA levels 3-
75 Additionally, the activation of SCD1 mRNA by clofibrate was inhibited 77% by cycloheximide administra
76 d in mice fed MCD formulas supplemented with clofibrate, which inhibits hepatic triglyceride accumula
77  of the cells to the classic PPAR activator, clofibrate, which resulted in a approximately 75% decrea
78 liferator activated receptor-alpha agonists, clofibrate, WY 14643, or linoleic acid, 45 min and 4 h a

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